实用医学杂志
實用醫學雜誌
실용의학잡지
THE JOURNAL OF PRACTICAL MEDICINE
2014年
11期
1693-1695
,共3页
王江友%李浪%周游%苏强%刘洋
王江友%李浪%週遊%囌彊%劉洋
왕강우%리랑%주유%소강%류양
阿托伐他汀%CD4+T淋巴细胞%程序性细胞死亡因子4%肿瘤坏死因子-α%白介素-10
阿託伐他汀%CD4+T淋巴細胞%程序性細胞死亡因子4%腫瘤壞死因子-α%白介素-10
아탁벌타정%CD4+T림파세포%정서성세포사망인자4%종류배사인자-α%백개소-10
Atorvastatin%CD4+T lymphocytes%Programmed cell death 4%Tumor necrosis factor-α%Interleukin-10
目的:研究阿托伐他汀在体外对人CD4+T淋巴细胞程序性细胞死亡因子4(PDCD4)表达的影响。方法:取20例健康志愿者的新鲜外周血,随机分为空白组、PHA刺激组、PHA+(1、5、10μmol/L)阿托伐他汀组,体外培养48 h后进行PDCD4 mRNA和蛋白及相关炎性因子的检测。结果:PHA刺激组PDCD4 mRNA、蛋白表达及上清TNF-α及IL-10浓度均升高(均P<0.05);经阿托伐他汀干预后,能够使PDCD4 mRNA、蛋白表达量及TNF-α浓度明显下降,而上清液IL-10浓度进一步增加;TNF-α与PDCD4蛋白呈明显的正相关(r=0.782,P<0.01),IL-10与PDCD4蛋白呈明显的负相关(r=-0.653,P<0.05)。结论:阿托伐他汀能够通过调控人CD4+T淋巴细胞PDCD4表达,从而发挥抗炎的作用。
目的:研究阿託伐他汀在體外對人CD4+T淋巴細胞程序性細胞死亡因子4(PDCD4)錶達的影響。方法:取20例健康誌願者的新鮮外週血,隨機分為空白組、PHA刺激組、PHA+(1、5、10μmol/L)阿託伐他汀組,體外培養48 h後進行PDCD4 mRNA和蛋白及相關炎性因子的檢測。結果:PHA刺激組PDCD4 mRNA、蛋白錶達及上清TNF-α及IL-10濃度均升高(均P<0.05);經阿託伐他汀榦預後,能夠使PDCD4 mRNA、蛋白錶達量及TNF-α濃度明顯下降,而上清液IL-10濃度進一步增加;TNF-α與PDCD4蛋白呈明顯的正相關(r=0.782,P<0.01),IL-10與PDCD4蛋白呈明顯的負相關(r=-0.653,P<0.05)。結論:阿託伐他汀能夠通過調控人CD4+T淋巴細胞PDCD4錶達,從而髮揮抗炎的作用。
목적:연구아탁벌타정재체외대인CD4+T림파세포정서성세포사망인자4(PDCD4)표체적영향。방법:취20례건강지원자적신선외주혈,수궤분위공백조、PHA자격조、PHA+(1、5、10μmol/L)아탁벌타정조,체외배양48 h후진행PDCD4 mRNA화단백급상관염성인자적검측。결과:PHA자격조PDCD4 mRNA、단백표체급상청TNF-α급IL-10농도균승고(균P<0.05);경아탁벌타정간예후,능구사PDCD4 mRNA、단백표체량급TNF-α농도명현하강,이상청액IL-10농도진일보증가;TNF-α여PDCD4단백정명현적정상관(r=0.782,P<0.01),IL-10여PDCD4단백정명현적부상관(r=-0.653,P<0.05)。결론:아탁벌타정능구통과조공인CD4+T림파세포PDCD4표체,종이발휘항염적작용。
Objective To investigate the influence of atorvastatin (Lipitor) on the expression of programmed cell death 4 (PDCD4) in human CD4+T lymphocytes in vitro. Methods Human CD4+T cells obtained from healthy individuals were activated with PHA and treated with atorvastatin. The mRNA and protein expression levels of PDCD4 were detected by real-time PCR and western-blot respectively. Results The stimulation of PHA obviously increased the mRNA and protein expression of PDCD4 and the secretion of those serum cytokines. The expression of PDCD4 and the production of serum TNF-α were significantly decreased, whereas the serum levels of IL-10 were significantly increased after treated by different concentration of atorvastatin. The serum secretion of TNF-α was positive correlation with the expression of PDCD4 through the linear related analysis (r=0.782, P<0.01), and the secretion of IL-10 was negative correlation with the expression of PDCD4 (r=-0.653, P<0.05). Conclusion The anti-inflammatory effects of atorvastatin are mediated by down regulating the expression of PDCD4 in CD4+T cells.